We Describe a case of ovarian serous cystadenoma having Sertoli-Leydig cell tumor, well differentiated, in the cystic septum. Well differentiated Sertoli-Leydig cell tumor coexisting with other tumor, including serous tumor, has not yet been described. In all cases of Sertoli-Leydig cell tumor with heterologous components or other tumors, the androblastomatous components are intermediately or poorly differentiated. The present case revealed a well differentiated Sertoli-Leydig cell tumor arising in a septum of serous cystadenoma, as a circumscribed nodule. With these findings, we discuss the possibility of this Sertoli-Leydig cell tumor, considered a mural nodule, which is well established in cystic common epithelial tumors of the ovary.
Adult ; Case Report ; Cystadenoma/*pathology ; Female ; Human ; Leydig Cells/pathology ; Male ; Ovarian Neoplasms/*pathology ; Sertoli Cells/pathology ; Sertoli-Leydig Cell Tumor/*pathology ; Support, Non-U.S. Gov't

OBJECTIVETo study the reversibility of di-n-butyl phthalate (DBP) effects on F(1) generation rat testes.

METHODSPregnant rats were treated with different dose of DBP (0, 50, 250 and 500 mg per kg per day) by gavage from GD1 to PND21. The adverse effects of DBP on testes of F(1) male rats in different developmental period (PND14, 21 and 70) were observed by anatomy and pathological methods.

RESULTSThere was no difference in rat testis weight and testis/body weight between DBP-treated group and the control. From the results of pathology and sertoli cell counting, comparing with the control, thinner seminiferous epithelium, decreased cell number and vacuole cells were observed in PND14 male DBP-treated rats. In PND21 rats, the number and form of sertoli cells were recovered and few exfoliated spermatogenic cells were found. When maturing to PND70, few rats were found irreversible damages such as seminiferous tubule degeneration, seminiferous epithelium atrophy, etc.

CONCLUSIONThese results suggest that adverse effects of DBP on young rat testes should be reversibility.

Animals ; Dibutyl Phthalate ; toxicity ; Female ; Male ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells ; pathology ; Testis ; drug effects ; pathology

OBJECTIVETo explore the relationship between germ cell apoptosis and the expression as well as the distribution of Sertoli cell vimentin induced by local exposure to heat.

METHODSLocal short-term exposure of prepubertal male rats testis to heat (43 degrees C for 15 min). Histochemical method was used to observe morphological characteristics of seminiferous tubule. The distribution and expression of Sertoli cell cytoskeletons were analyzed by immunohistochemistry and germ cell apoptosis was evaluated by TUNEL technique at different hour-intervals.

RESULTSAfter 2 h and 4 h heat exposure, the disattachment phenomenon between Sertoli cell and spermatogonia occurred. Spermatogonia arranged in disorder and displaced away from the basement membrane of seminiferous tubules. Immunohistochemical staining showed that vimentin positive staining was seen radiating from the Sertoli cell perinuclear region with apical "spoke-like" pattern in controls. There was an intense vimentin immunoreactivity surrounding Sertoli cell nuclei along with the collapse of the apical extensions in 2 h group, but no significant difference compared with the controls. The expressions of vimentin in 12 h and 24 h groups were higher than those of the controls (P <0.01), respectively. TUNEL showed that incidence of apoptosis was observed to increases markedly in 12 h and 24 h groups, but it was found that the incidences of apoptotic events were decreased in these two groups compared with the controls.

CONCLUSIONThe changes of expression and distribution of Sertoli cell vimentin filaments correlate with the increased germ cell apoptosis. Local heat may disrupt spermatogenesis by injuring Sertoli cell directly.

Animals ; Apoptosis ; Hot Temperature ; In Situ Nick-End Labeling ; Male ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells ; metabolism ; Spermatozoa ; pathology ; Vimentin ; biosynthesis

Mucinous neoplasms occur rarely in association with cystic teratoma, Sertoli-Leydig cell tumor, granulosa cell tumor or carcinoid tumor. Several cases of an ovarian stromal tumor with minor sex-cord elements have been reported in the literatures. However, there has been no report about an ovarian mucinous neoplasm coexisting with a stromal tumor with sex-cord elements yet. We report a case of an ovarian neoplasm composed of both mucinous cystadenoma and stromal tumor with minor sex-cord elements in a 58-yr-old female. The ovary including the mass measured 5 cm in size. On section, it revealed an unilocular cyst (4.5 cm in diameter) filled with mucinous fluid. There was a round, yellow, solid nodule, 1.5 cm in diameter within the wall. Microscopically, the cyst was lined by a single layer of endocervical mucinous epithelium and the nodule was composed of spindle cells showing an intersecting and whorled arrangement. There were cell nests showing polygonal shape with abundant cytoplasm among the spindle cells. They showed immunoreactivity for inhibin and did not have any connection with the adjacent mucinous epithelium. Therefore, we interpret the mucinous cystadenoma as having arisen de novo.
Cystadenoma, Mucinous/chemistry/*pathology ; Female ; Human ; Inhibin/analysis ; Middle Age ; Ovarian Neoplasms/chemistry/*pathology ; Sertoli-Leydig Cell Tumor/pathology ; Stromal Cells/*pathology

Diabetes is a metabolic disease caused by complicated factors, and its damage to the male reproductive system is threatening men's health. This article reviews the pathophysiological changes in the diabetes-damaged male reproductive system and the mechanism of these changes. Oxidative stress induced by hyperglycemia plays an important role in working damage to the reproductive system of diabetic males, for which some anti-oxidative substances may prove to be an effective cure.
Androgen-Binding Protein ; biosynthesis ; Animals ; Diabetes Mellitus ; pathology ; physiopathology ; Free Radicals ; Humans ; Leydig Cells ; metabolism ; Male ; Oxidative Stress ; Rats ; Sertoli Cells ; secretion ; Testis ; pathology ; Testosterone ; biosynthesis

AIMTo determine the involvement of apoptotic cell death in postnatal pathogenesis in mutant strain of hypogonadic (hgn/hgn) rats testes. We evaluated the numbers and types of cells undergoing apoptotic cell death.

METHODSTissue sections were stained by the TUNEL method for in situ detection of apoptotic cells, with specific antibodies used as markers of testicular somatic and germ cells.

RESULTSWe found that apoptosis in the hgn/hgn testes during the early postnatal period occurred primarily in Sertoli cells, which should actively proliferate during this stage of differentiation. These findings strongly suggest that the normal allele of hgn is involved in the direct or indirect control of differentiation and proliferation of Sertoli cells.

CONCLUSIONTo our knowledge, this is the first report demonstrating early postnatal apoptosis of Sertoli cells, suggesting that the hgn/hgn rat is a unique model for the study of Sertoli cell deficiency.

Aging ; Animals ; Apoptosis ; Cell Death ; Hypogonadism ; pathology ; In Situ Nick-End Labeling ; Male ; Rats ; Rats, Inbred Strains ; Sertoli Cells ; pathology ; physiology ; Testis ; growth & development ; pathology

OBJECTIVETo explore whether microwave radiation may cause injury of primary cultured Sertoli cells.

METHODSThe model of primary cultured Sertoli cells in vitro was established, which was radiated by microwave with average power density 0, 30 and 100 mW/cm(2) for five minutes. The changes of cell cycle, apoptosis and death, and intracellular Ca2+ concentration in the Sertoli cells were measured at sixth hours through Annexin V-PI double labeling and Fluo-3-AM labeling, flow cytometry combined with laser scanning confocal microscopy after microwave exposure.

RESULTSThe numbers of Sertoli cells were obviously reduced in G0-G1 and G2-M phase (62.57% +/- 3.22% and 8.25% +/- 1.75%) and increased in S phase (29.17% +/- 4.87%) compared with the control groups (79.18% +/- 0.24%, 11.17% +/- 0.50% and 9.64% +/- 0.62%) (P < 0.05 or P < 0.01), but the changes of rate of apoptosis and death and intracellular Ca2+ concentration showed no difference at 6 h after exposure to 30 mW/cm(2) microwave. There was a significant increase in the Sertoli cell counts of G0-G1 phase (87.69% +/- 1.32%), and decrease in the Sertoli cell counts of G2-M and S phase (7.41% +/- 0.60% and 4.87% +/- 0.91%) (P < 0.01). There was also a significant increase in intracellular Ca2+ concentration and rate of apoptosis and death (P < 0.05 or P < 0.01) at 6 h after exposure to 100 mW/cm(2) microwave.

CONCLUSION100 mW/cm(2) microwave radiation may cause growth inhibition and increase of apoptosis and death in the primary cultured Sertoli cells. The increase of intracellular Ca2+ concentration is one of the injury mechanisms.

Animals ; Apoptosis ; radiation effects ; Calcium ; metabolism ; Cell Cycle ; radiation effects ; Cells, Cultured ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Wistar ; Sertoli Cells ; metabolism ; pathology ; radiation effects

OBJECTIVETo explore the effects of Di (2-ethylhexyl) phthalate (DEHP) on the testis and testicular gubernaculum of fetal KM mice in vivo and to investigate the mechanism of DEHP-induced cryptorchidism.

METHODSThirty healthy pregnant KM mice were randomly and equally divided into a blank control group, a corn oil control group and a DEHP group. The pregnant mice in the latter group were exposed to DEHP by gavage at the dose of 500 mg/kg body weight per day from gestation day 12 (GD12) through gestation day 19 (GD19). The effects of DEHP were observed on the number of fetuses per pregnancy, the ratio of male to female pups, the weight of the testis, the morphology and location of the testis and gubernaculum, the relative testis-bladder neck distance (TBD) and cranial suspensory ligament (CSL) residual. The expressions of the androgen receptor (AR), estrogen receptor (ER) and actin and proliferating cell nuclear antigen (PCNA) in the gubernaculum were detected by immunohistochemistry.

RESULTSDEHP reduced the testis weight and TBD, induced different degrees of testis maldescent, but produced no obvious effect on the body weight, the number of fetuses per pregnancy, the sex ratio and the testis gubernacular morphology. Under the light microscope, hypotrophy was seen in all the testis seminiferous tubules, spermatogenic cells and Sertoli cells, marked Leydig cell hyperplasia was noted, and the positive expression of AR in the gubernaculum was decreased in the DEHP group (P < 0.01).

CONCLUSIONDEHP could cause dysfunction of the testis gubernaculum via its anti-androgen effect, induce cryptorchidism, and cause dysplasia and dysfunction of Sertoli cells, Leydig cells and spermatogenic cells in fetal mice.

Animals ; Diethylhexyl Phthalate ; pharmacology ; Female ; Fetus ; drug effects ; Leydig Cells ; drug effects ; Male ; Mice ; Mice, Inbred Strains ; Pregnancy ; Sertoli Cells ; drug effects ; Testis ; cytology ; drug effects ; pathology

OBJECTIVETo evaluate the effects of Attractin (Atrn) silence on the anti-oxidative and anti-apoptotic abilities of TM4 Sertoli cells and its influence on the expressions of superoxide dismutase (SOD) and caspase6 in the cells.

METHODSWe observed the apoptotic indexes of TM4 Sertoli cells with normal expression (control), partial deletion, and complete deletion of the Atrn gene (psiRNA-TM4, psiAtrn-TM4, and mu-SC). We determined the mRNA and protein expressions of SOD and caspase6 by Q-PCR and Western blot, measured the SOD activity and malondialdehyde (MDA) contentby spectrophotometry, and detected the apoptotic index of the cells by TUNEL.

RESULTSCompared with psiRNA-TM4, after inhibition of the Atrn expression, the Sertoli cells in the psiAtrn-TM4 and mu-SCgroups showed significantly decreased expressions ofSOD mRNA (70.76% and 92.58%) and protein (65.11% and 71.0%) (both P < 0.05). The levels of caspase 6 mRNA and protein were increased 5.28 and 3.40 times in the psiAtrn-TM4 and 2.97 and 2.50 times in the mu-SCgroup as compared with the normal control (both P < 0.05). Atrn deletion markedly increased the apoptotic indexes of the cells in the psiAtrn-TM4 and mu-SC groups by 16.22% and 22.03% (P < 0.05) and reduced the activity of SOD by 23.00% and 39.37% (P < 0.05); it also elevated the level of MDA by 155.22% (P < 0.05).

CONCLUSIONThe Atrn gene exerts influence on the function of Sertoli cells in multiple ways, in which antioxidative stress and apoptosis regulation may play an important role.

Animals ; Apoptosis ; Caspase 6 ; metabolism ; Cells, Cultured ; Gene Deletion ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Oxidative Stress ; Sertoli Cells ; metabolism ; pathology ; Superoxide Dismutase ; metabolism

AIMTo determine the frequency of genetic deletions within the azoospermia factors in Egyptian infertile males.

METHODSThe Yq microdeletions in 33 infertile males with undetectable chromosomal anomalies were examined by mutiplex polymerase chain reaction (PCR). Deletions were confirmed using single PCR amplifications.

RESULTSFour out of the total 33 (12 %) men had Yq(11) microdeletions, thus supporting the average reported figures in other populations. Three of those 4 cases had single short tandem sequence deletions with discrete histological findings of their testes. Single sY272 deletion within AZFc was associated with Sertoli cell only syndrome, whereas a patient with isolated sY84 deletion within AZFa had immature testicular structure. The remaining case had a large deletion in AZFa-c and short stature.

CONCLUSIONThe present study supports the hypothesis that the Yq(11) encompasses genetic determinants of stature besides genes controlling spermatogenesis.

Adult ; Chromosomes, Human, Y ; genetics ; Egypt ; Follicle Stimulating Hormone ; blood ; Gene Deletion ; Humans ; Infertility, Male ; genetics ; pathology ; Luteinizing Hormone ; blood ; Male ; Polymerase Chain Reaction ; Sertoli Cells ; pathology ; Syndrome ; Testis ; pathology ; Testosterone ; blood